Reactivation of latent herpes simplex many result in visually disabling keratitis and is the most common cause of corneal blindness due to an infectious agent in the United States. We have developed a murine model of recurrent herpetic keratitis using a naturally occurring stimulus -- ultraviolet B light -- that consistently results in recoverable virus at the ocular surface in at least 70% of irradiated latently-infected animals. It is now proposed to further characterized and exploit the model with regard to the following Specific Aims which are critical to our understanding of the basic biology of herpetic reactivation in vivo: (1) to characterize viral immediate-early gene expression in trigeminal ganglia neurons in the period following UV-B induced reactivation in vivo; (2) identification of HSV-1 genes and promoters essential for viral reactivation in vivo by creation of intratypic recombinants and selection in the UV-B reactivation model; (3) to utilize antibodies to neuropeptides and cell surface carbohydrates to characterize the neuronal cell types in the trigeminal ganglia in which latency is established an in which viral reactivation occurs following the UV-B stimulus. This information will greatly enhance our understanding of viral reactivation and may be useful in the future in the directed design of antiviral drugs, as well as prophylactic agents to prevent viral reactivation itself.